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作 者:马盼 贾云宏 Pan Ma;Yun-hong Jia(Graduate School,Jinzhou Medical University,Jinzhou,Liaoning 121001,China;College of Pharmacy,Jinzhou Medical University,Jinzhou,Liaoning 121001,China)
机构地区:[1]锦州医科大学研究生学院,辽宁锦州121001 [2]锦州医科大学药学院,辽宁锦州121001
出 处:《中国现代医学杂志》2018年第19期23-27,共5页China Journal of Modern Medicine
摘 要:目的探讨索拉非尼对体外培养MHCC97-H肝癌细胞中肝再生磷酸酶3(PRL-3)表达水平的影响,以及对肝癌细胞侵袭力的作用。方法在24、48及72 h测定经不同浓度梯度索拉非尼处理MHCC97-H肝癌细胞增殖抑制率以筛选合适的干预浓度和时间。采用MHCC97-H肝癌细胞培养传代,用索拉非尼干预处理,瑞氏吉姆萨法染色观察形态学变化,MTT法检测其增殖抑制率,Western blot法检测PRL-3蛋白表达水平,Transwell实验检测癌细胞侵袭力。结果该实验索拉非尼体外最佳干预实验浓度和时间分别为16μmol/L和48 h;索拉非尼能诱导肝癌细胞株MHCC97-H的凋亡,肝癌细胞增殖抑制率与时间和剂量呈正相关。经索拉非尼作用后PRL-3蛋白也出现不同程度下降,肝癌细胞侵袭能力明显下降。结论索拉非尼能降低MHCC97-H肝癌细胞株中PRL-3蛋白表达水平,降低肿瘤细胞侵袭力,从而诱导肝癌细胞凋亡;索拉非尼降低癌细胞的侵袭可能是通过下调PRL-3蛋白进行。Objective To investigate the effect of Sorafenib on the proliferation and apoptosis of MHCC97-H human hepatocellular carcinoma cells in vitro,as well as its effect on expression of PRL-3 protein and cell invasiveness.Methods Different concentrations of Sorafenib were applied to MHCC97-H human hepatocellular carcinoma cells,and MTT assay was used to observe the inhibitory effect of Sorafenib on the cell proliferation at 24,48 and 72 h to screen the optimum concentration of Sorafenib and intervention time.Giemsa staining was used to observe the morphological changes of the cells.Western blot was used to detect the protein expression of PRL-3.Transwell assay was used to detect the invasiveness of the tumor cells.Results The optimum concentration and time of Sorafenib intervention were 16μmol/L and 48 h,respectively.Sorafenib induced apoptosis of MHCC97-H hepatocellular carcinoma cells.The inhibition rate of MHCC97-H cell proliferation was positively correlated with time and dosage.Sorafenib also decreased PRL-3 protein expression to different extent.After the expression of PRL-3 decreased,the hepatocellular carcinoma cell invasion ability was significantly inhibited.Conclusions Sorafenib can reduce the expression level of PRL-3 protein in MHCC97-H hepatocellular carcinoma cell line,and decrease the invasiveness of the cells,so as to induce the apoptosis of hepatocellular carcinoma cells.Its inhibition of cancer cell migration may be mediated by down-regulation of PRL-3 protein.
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